Selective reduction in neural responses to high calorie foods following gastric bypass surgery

Abstract

Objective: To investigate changes in neural activation and desire to eat in response to appetitive cues from pre- to postbariatric surgery for obesity.

Background: Roux-en-Y gastric bypass (RYGB) is the most common bariatric procedure. However, the mechanisms of action in RYGB are not well understood. A significant proportion of the resulting reduction in caloric intake is unaccounted for by the restrictive and malabsorptive mechanisms and is thought to be mediated by neuroendocrine function. Numerous investigations of postsurgical changes in gut peptides have resulted; however, changes in neural activation after RYGB surgery have not been previously investigated.

Methods: Functional magnetic resonance imaging and verbal rating scales were used to assess brain activation and desire to eat in response to high- and low-calorie food cues in 10 female patients 1-month pre- and post-RYGB surgery.

Results: Postsurgical reductions in brain activation were found in key areas within the mesolimbic reward pathway, which were significantly more pronounced in response to food cues that were high (vs. low) in caloric density. These changes mirrored concurrent postsurgical reductions in desire to eat, which were also greater in response to food cues that were high versus low in caloric density (P = 0.007).

Conclusions: Findings support the contention that RYGB surgery leads to substantial changes in neural responses to food cues encountered in the environment, provide a potential mechanism for the selective reduction in preferences for high-calorie foods, and suggest partial neural mediation of changes in caloric intake seen after RYGB surgery.

FIGURE 1

Axial slices depicting areas in which activation was greater presurgery as compared to postsurgery across stimuli conditions. Relative to low-ED foods (bottom row), larger postsurgical reductions in conjoint (visual and auditory) activation (pre > postsurgery) in response to high-ED foods (top row) are seen in VTA (z = −10), ventral striatum (z = −4), putamen and lentiform nucleus (z = 2) posterior cingulate (z = 28, left clusters) and dmPFC (z = 28, rightmost cluster). Montreal Neurological Institute coordinates for the axial slices are given below the statistical maps. The color bar represents t values. For display purposes, activation maps are shown without a cluster extent threshold.

FIGURE 2

Coronal and sagittal slices depicting areas in which the difference between conjoint activation in response to high- and low-ED foods (high-ED–low-ED contrast) was greater presurgery as compared to postsurgery. Montreal Neurological Institute coordinates are given in upper right corner of each panel. The color bar represents t values. The largest clusters (k > 80) were seen in the dlPFC (y = 42; topmost cluster), ventrolateral PFC (vlPFC; y = 42; bottom cluster), ventral striatum (y = 4; bottom 2 clusters), putamen and lentiform nucleus (y = 0; bottom cluster), and dmPFC (x = 4; rightmost cluster). A small cluster (k = 20) was also observed in the VTA (x = 4; white arrow). Peak MNI coordinates for the above regions are listed in Table 1.

FIGURE 3

The difference between the desire to eat following exposure to high-ED relative to low-ED foods (high-ED–low-ED) presurgery (11.5 ± 10) was greater than the non-significant high-ED to low-ED difference postsurgery (0.5 ± 4.2), F (1,9) = 11.9, P = 0.007. ^*P < 0.05. ^**P < 0.01.